Cytochrome c release and apoptosis induced by mitochondrial targeting of nuclear orphan receptor TR3
H Li, SK Kolluri, J Gu, MI Dawson, X Cao, PD Hobbs… - Science, 2000 - science.org
H Li, SK Kolluri, J Gu, MI Dawson, X Cao, PD Hobbs, B Lin, G Chen, J Lu, F Lin, Z Xie…
Science, 2000•science.orgTR3, an immediate-early response gene and an orphan member of the steroid-thyroid
hormone-retinoid receptor superfamily of transcription factors, regulates apoptosis through
an unknown mechanism. In response to apoptotic stimuli, TR3 translocates from the nucleus
to mitochondria to induce cytochrome c release and apoptosis. Mitochondrial targeting of
TR3, but not its DNA binding and transactivation, is essential for its proapoptotic effect. Our
results reveal a mechanism by which a nuclear transcription factor translocates to …
hormone-retinoid receptor superfamily of transcription factors, regulates apoptosis through
an unknown mechanism. In response to apoptotic stimuli, TR3 translocates from the nucleus
to mitochondria to induce cytochrome c release and apoptosis. Mitochondrial targeting of
TR3, but not its DNA binding and transactivation, is essential for its proapoptotic effect. Our
results reveal a mechanism by which a nuclear transcription factor translocates to …
TR3, an immediate-early response gene and an orphan member of the steroid-thyroid hormone-retinoid receptor superfamily of transcription factors, regulates apoptosis through an unknown mechanism. In response to apoptotic stimuli, TR3 translocates from the nucleus to mitochondria to induce cytochrome c release and apoptosis. Mitochondrial targeting of TR3, but not its DNA binding and transactivation, is essential for its proapoptotic effect. Our results reveal a mechanism by which a nuclear transcription factor translocates to mitochondria to initiate apoptosis.
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